Table 1.
Component Type | Complement Component (s) | Role in Cancer | Experimental Setting | Cell Line(s) | In Vivo Model | Mechanism | Ref |
---|---|---|---|---|---|---|---|
Complement effectors and receptors | C1q | Anti-tumor | In vitro | SKOV3 | - | Induction of apoptosis | [100] |
gC1qR | Anti-tumor | In vitro | C33a, SiHa | - | Induction of apoptosis | [101] | |
gC1qR | Anti-tumor | In vitro | SKOV3, CAOV-3 |
- | Induction of apoptosis after paclitaxel treatment | [102] | |
C3 and C5aR1 | Pro-tumor | In vivo | - | Spontaneous model in C57BL/6 TgMISIIR-Tag mice | Inhibition of angiogenesis | [103] | |
C3aR and C5aR1 | Pro-tumor | In vivo | ID-8 VEGF | Syngenic model in C57BL/6 mice | Autocrine stimulation of tumor growth | [104] | |
C3 | Pro-tumor | In vivo | ID-8 VEGF | Syngenic model in C57BL/6 mice | Autocrine promotion of EMT | [105] | |
C3 and C5aR1 | Anti-tumor | In vivo | TC-1 | Syngenic model in B6.SJL-PtprcaPep3b/BoyJ mice | Promotion of T-cell homing | [106] | |
C5a | Anti-tumor Pro-tumor |
In vivo | SKOV-3 | Xenograft model in SCID mice | Dose-dependent effect on tumor growth | [107] | |
Complement regulators | CD59, CD46, FH, and FHL-1 | Pro-tumor | In vitro | Caov-3, SK-OV-3, SW626, PA-1, HUV-EC-C |
- | Functional complement activation and regulation occurs locally in ascites | [64] |
CD55 | Pro-tumor | In vivo | SK-OV-3 | Xenograft model in SCID* mice | Blockade of CD55 leads to improved efficacy of mAb therapy | [108] | |
CD55 | Pro-tumor | In vivo | A2780, TOV112, CP70, HEC1a |
Xenograft model in SCID mice | Silencing of CD55 restores sensitivity to chemotherapy | [109] | |
CD59 | Pro-tumor | In vivo | A2780 | Xenograft model in SCID mice | Silencing of CD59 reduces tumor growth | [110] | |
CD59 | Pro-tumor | In vitro | SK-OV-3 | - | Neutralization improves CDC mediated by mAb therapy | [111] | |
CD46 and CD59 | Pro-tumor | In vitro | IGROV1, OVCAR3, SKOV3, OAW42, INTOV1, INTOV2 |
- | Neutralization improves CDC mediated by mAb therapy | [112] | |
CD46, CD55, and CD59 | Pro-tumor | In vitro | SK-OV-3 | - | Silencing of CRPs leads to improved efficacy of mAbs | [113] | |
FH, FHL-1, and sCD46 | Pro-tumor | In vitro | SK-OV-3, Caov-3, PA-1, SW626 |
- | Resistance to CDC | [114] |
EMT: epithelial-mesenchymal transition, SCID: severe combined immunodeficient, mAb: monoclonal antibody, CDC: complement-dependent cytotoxicity.